Evidence map›Paper›PMID 28348240›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Endothelial transcription factor KLF2 negatively regulates liver regeneration via induction of activin A.

Yosif Manavski, Tobias Abel, Junhao Hu, Dina Kleinlützum, Christian J Buchholz, Christina Belz, Hellmut G Augustin, Reinier A Boon, Stefanie Dimmeler

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  4. Cells · 2025
    Review
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  6. Article
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  8. Review
  9. Article
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  11. Review
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  13. Biomechanics in liver regeneration after partial hepatectomy.Frontiers in bioengineering and biotechnology · 2023
    Review
  14. Cellular crosstalk during liver regeneration: unity in diversity.Cell communication and signaling : CCS · 2022
    Review
  15. Review
  16. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Yosif ManavskiInstitute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe-University, 60590 Frankfurt, Germany.
Tobias AbelMolecular Biotechnology and Gene Therapy, Paul-Ehrlich-Institut, 63225 Langen, Germany.
Junhao HuDepartment of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), 69120 Heidelberg, Germany.
Dina KleinlützumMolecular Biotechnology and Gene Therapy, Paul-Ehrlich-Institut, 63225 Langen, Germany.
Christian J BuchholzMolecular Biotechnology and Gene Therapy, Paul-Ehrlich-Institut, 63225 Langen, Germany.
Christina BelzInstitute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe-University, 60590 Frankfurt, Germany.
Hellmut G AugustinDepartment of Vascular Oncology and Metastasis, German Cancer Research Center (DKFZ-ZMBH Alliance), 69120 Heidelberg, Germany.
Reinier A BoonInstitute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe-University, 60590 Frankfurt, Germany.ORCID 0000-0001-7944-9748
Stefanie DimmelerInstitute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe-University, 60590 Frankfurt, Germany; dimmeler@em.uni-frankfurt.de.
Goethe University Frankfurt · DEPaul Ehrlich Institut · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial cells (ECs) not only are important for oxygen delivery but also act as a paracrine source for signals that determine the balance between tissue regeneration and fibrosis. Here we show that genetic inactivation of flow-induced transcription factor Krüppel-like factor 2 (KLF2) in ECs results in reduced liver damage and augmentation of hepatocyte proliferation after chronic liver injury by treatment with carbon tetrachloride (CCl

Indexed as

ActivinsAnimalsCarbon TetrachlorideCell ProliferationChemical and Drug Induced Liver InjuryEndothelial CellsGene Expression RegulationHepatocytesHumansHuman Umbilical Vein Endothelial CellsKruppel-Like Transcription FactorsLiverLiver CirrhosisLiver RegenerationMice, Transgenicactivin AActivinsCarbon TetrachlorideKlf2 protein, mouseKruppel-Like Transcription Factorsactivin AKLF2vascular niche

Identifiers

PMID28348240
PMCPMC5393189
OpenAlexW2600586351

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.